碘酸钾和碘化钾对小鼠抗氧化能力影响的对比研究

目的用接近于流行病学调查现场实际的碘水平,研究碘酸钾、碘化钾对小鼠抗氧化能力的影响。方法将小鼠按体质量随机分为基础饲料组(NG)、适碘酸钾组(NO)、高碘酸钾组(HO)、高碘化钾组(HI),喂养90d后,测定甲状腺质量和血液中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)活力以及脂质过氧化产物(MDA)水平,在光镜和电镜下观察甲状腺形态结构的变化。结果HO和HI组小鼠甲状腺出现胶质样肿大、绝对质量和相对质量增加。与NG组比较,HO组MDA明显上升,SOD/MDA比值明显降低;HI组MDA、SOD/MDA比值无明显变化;NO组上述各项指标无明显变化。结论当饮水中碘为100μg/L时,碘酸钾与碘化钾均可引起小鼠甲状腺肿大,并且碘酸钾使小鼠抗氧化能力减弱,而碘化钾没有使小鼠抗氧化能力减弱,说明机体对碘化钾的耐受性低。     

碘酸钾和碘化钾对碘缺乏大鼠甲状腺抗氧化能力的影响

目的 研究碘酸钾和碘化钾两种碘剂对碘缺乏大鼠甲状腺抗氧化能力的影响。方法 Wistar大鼠低碘喂养3个月，复制出低碘模型后，随机分为4组：适碘碘化钾组（NI），适碘碘酸钾组（NO），高碘碘化钾组（HI），高碘碘酸钾组（HO），喂养22周后测定尿碘排泄情况、甲状腺重量、血清甲状腺激素水平和甲状腺组织抗氧化能力改变，观察甲状腺形态变化。结果 HO与HI两组补碘后尿碘显升高；与NI组相比，HO组甲状腺湿重及相对重量均明显增加，HI组甲状腺相对重量明显增加，与NI相比，HO、HI组T3显升高；与NI组相比，NO、HO、HI组GPX、SOD和TAOC均显降低，HO组MDA显升高，但NO、HI组MDA无明显升高；与HI组相比，HO组的GPX、TAOC显降低。结论 碘缺乏大鼠补充大剂量碘酸钾或大剂量碘化钾后，甲肿消退速度慢；无论补充生理或大剂量碘剂，与碘化钾相比，补充碘酸钾甲状腺抗氧化物酶持续降低，大剂量碘酸钾导致甲状腺MDA含量升高。     

碘酸钾和碘化钾对碘缺乏大鼠大脑抗氧化能力的影响

目的：研究不同剂量碘酸钾和碘化钾对碘缺乏大鼠大脑抗氧化能力的影响，方法：120只Wistar大鼠低碘喂养3个月后随机分为4组：适碘碘化钾组（NI）、适碘碘酸钾组（NO）、高碘碘化钾组（HI）、高碘碘酸钾组（HO）、喂养22周后测定全脑重量，抗氧化能力。结果：4组大鼠全脑重量差异无显著意义；与NI组相比，NO，HO组GSH－Px,SOD,TAOC显著降低（P＜0．05），MDA显著升高（P＜0．05），HI组各项指标差异均无显著意义；与HI组相比，HO组GSH－Px，SOD，TAOC显著降低（P＜0．05），MDA显著升高（P＜0．05）。结论：与补充相同剂量的碘化钾相比，碘缺乏大鼠补充适量或大剂量碘酸钾后，脑组织抗氧化能力显著降低。     

不同剂量碘酸钾和碘化钾对缺碘大鼠甲状腺肿回缩效果的影响

目的 观察补充不同剂量和剂型的碘剂对甲状腺肿回缩的效果和甲状腺功能的影响。方法 成功复制缺碘性甲状腺肿(甲肿)动物模型后，分别补给适量(1倍、0．26mg／L)，5倍(1．30mg／L)和50倍(13．00mg/L)于适量碘的碘酸钾和碘化钾3月。结果 各实验组甲状腺相对重量较低碘组明显下降，但均未能恢复至正常水平，且随补碘剂量增加，甲肿恢复呈渐差趋势；各组尿碘排泄情况基本与摄人碘量呈平行关系，各实验组甲状腺组织碘低于正常对照组，且各实验组之间无显著差别；各实验组血清TT4水平显著高于正常对照组，1倍和5倍补碘组甲状腺组织TT4水平明显高于50倍补碘组和正常对照组；相同的补碘水平上，碘酸钾和碘化钾组各项指标均未见显著差异。结论 补碘对甲肿回缩均有一定效果，但适量碘组效果最佳；5倍补碘组甲肿消退虽稍差于适量补碘组，但差别无统计学意义，提示5倍于适量碘仍然是比较安全的；50倍于适量碘组甲肿消退明显减慢，提示过高剂量补碘不利于甲肿回缩；相同的补碘水平上，碘酸钾和碘化钾对甲肿回缩的效果是一致的，证明碘酸钾补碘效果可靠。     

合成饲料复制小鼠高碘性甲状腺肿动物模型

目的 应用合成饲料复制小鼠高碘性甲状腺肿动物模型。方法 将昆明种小鼠按体质量随机分为对照（NI）组、高碘（HI）组，饲以美国营养学会推荐配方的合成饲料，分别饮用碘酸钾配制的含碘量为50、3000μg／L的去离子水。喂养1、3、6个月后，称小鼠体质量和甲状腺质量，放免法测定血清甲状腺激素水平，光镜下观察小鼠甲状腺形态学变化。结果 与NI组相比，1、3、6个月时HI组小鼠甲状腺绝对质量和相对质量明显增高（P〈0．05或〈0．01）；1、6个月时HI组T3水平升高（P〈0．01或〈0．05），而T4水平未见明显改变（P〉0．05）。3、6个月时HI组光镜下各观察9例小鼠甲状腺，呈现胶质潴留性甲状腺肿大者分别为6、8例，NI组分别观察了9、12例小鼠甲状腺，未见甲状腺肿大者，两组比较差异有统计学意义（P〈0．05或〈0．01）。结论 采用美国营养学会推荐的合成饲料配方，可复制出高碘性甲状腺肿动物模型。     

不同剂量碘酸钾和碘化钾对缺碘性大鼠甲状腺肿治疗效果的实验观察

目的观察不同剂量和剂型的碘对缺碘性大鼠甲状腺肿(甲肿)的治疗效果和对甲状腺功能的影响.方法在成功复制缺碘性甲肿动物模型的基础上,分别给予1倍(适量碘)、5倍和50倍于适量碘的碘酸钾和碘化钾6种措施进行干预治疗3月,取材测定各项指标.结果各治疗组甲状腺相对重量均较低碘组明显下降,但均未能恢复至正常水平,且随补碘剂量增加,甲肿恢复呈渐差趋势;各组尿碘排泄情况基本与摄入碘量呈平行关系,各治疗组甲状腺组织碘含量明显低于正常对照组,且各治疗组之间比较差异无显著意义;各治疗组血清T4水平显著高于正常对照组,1倍和5倍补碘组甲状腺组织T4水平明显高于50倍补碘组和正常对照组;相同的补碘水平上,碘酸钾和碘化钾组各项指标差异均无显著意义.结论①各治疗组对甲肿均有一定治疗效果,但适量碘治疔甲肿效果最佳;5倍补碘组甲肿消退虽稍差于适量补碘组,但差别无统计学意义,提示5倍于适量碘仍然是比较安全的;50倍于适量碘组甲肿消退明显减慢,提示过高剂量补碘不利于甲肿恢复;②相同的补碘水平上,碘酸钾和碘化钾治疗甲肿的效果是一致的,证明碘酸钾补碘安全可靠.     

碘酸钾和碘化钾对大鼠抗氧化能力和超微结构的影响

目的观察两种碘剂及不同剂量,对大鼠抗氧化能力和超微结构的影响.方法先用低碘饲料和去离子水喂养120只Wistar大鼠3个月复制低碘动物模型.随机分为4组适碘碘酸钾(KIO3)组(NO),适碘碘化钾(KI)组(NI),分别饮含碘量为230μg/L的KIO3和KI去离子水;高碘KIO3组(HO)和高碘KI组(HI)饮水碘含量分别为前2组的100倍.喂养22周后处死,测定甲状腺、视网膜、脑和肾脏的谷胱甘过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、总抗氧化能力(TAOC)和丙二醛(MDA)的含量.光镜和电镜观察脑、视网膜、甲状腺的形态学变化.结果甲状腺NO及HO组GSH-Px活性分别显著低于NI和HI组,NO组SOD活性和HO组TOAC活性分别显著低于NI和HI组;脑NO和HO组GSH-Px、SOD、TOAC组的活性分别显著低于NI和HI组,而MDA的含量则均显著高于NI和HI组,表明KIO3使脑组织多项抗自由基酶活性的损伤,已经进入失代偿阶段;视网膜NO和HO组TOAC的活性均显著低于NI和HI组.形态学观察,光镜下HO、HI组甲状腺滤泡明显增大,上皮细胞多为扁平状,滤泡腔内充满丰富浓染胶质.在电镜下NI组大脑神经元未见异常,NO组神经元胞浆多数粗面内质网(RER)池扩张,核皱缩,树突水肿.HI组神经元有较多呈暗细胞变,RER池扩张,核染色质高度分散均匀.HO组神经元呈高度暗细胞变,胞浆皱缩,RER池扩张,线粒体变性,核内陷.结论相同碘量的生理剂量和大剂量KIO3组抗氧化能力和病理损伤程度比KI组更为严重.NI组损伤的程度为最轻,而HO组则严重.提示,KIO3碘盐防治IDD的安全性,应引起有关方面关注.     

不同剂量碘酸钾与碘化钾治疗Wistar大鼠缺碘性甲状腺肿效果观察

目的探讨不同剂量碘酸钾和碘化钾治疗Wistar大鼠缺碘性甲状腺肿的效果。方法选取80只健康Wistar大鼠,随机分为A组(70只)和B组(10只)。A组大鼠产生明显甲状腺肿后将其随机分为7组,每组10只。在成功复制缺碘性甲状腺肿大鼠动物模型后,以单倍碘(0.26mg/L)、5倍和50倍的碘酸钾和碘化钾六种方法补碘,分别在1、3个月后检测大鼠绝对和相对甲状腺重量、尿碘含量、组织碘含量、细胞面积/视场面积和胶质面积/视场面积情况。结果各KI组和KIO3组大鼠的绝对和相对甲状腺重量均显著低于对照组,高于B组,差异有统计学意义(P0.05);50倍KI组和50倍KIO_3组大鼠的甲状腺绝对和相对重量显著高于其他KI组和KIO_3组,差异有统计学意义(P0.05)。各KI组和KIO_3组大鼠的尿碘水平显著高于对照组,差异有统计学意义(P0.05);不同补碘水平间的尿碘水平比较差异有统计学意义(P0.05);同一补碘水平的KI组和KIO_3组尿碘水平比较差异无统计学意义(P0.05);各组补碘3个月的尿碘水平均显著高于补碘1个月,差异有统计学意义(P0.05)。各KI组和KIO_3组大鼠的甲状腺组织碘含量显著高于对照组,低于B组,差异有统计学意义(P0.05)。各KI组和KIO_3组的细胞面积/视场面积显著低于对照组,差异有统计学意义(P0.05);在补碘后3个月后,50倍KI组和50倍KIO_3组的细胞面积/视场面积显著低于其余各KI组和KIO3组,差异有统计学意义(P0.05);各KI组和KIO_3组的胶质面积/视场面积显著高于对照组,差异有统计学意义(P0.05)。结论不同剂量碘酸钾和碘化钾均可有效纠正缺碘性甲状腺肿,相同补碘剂量之间的效果相似,而大剂量补碘会损伤甲状腺,适量KIO_3对于纠正碘缺乏具有较好效果,且安全性高。     

碘与酪氨酸交互作用对小鼠甲状腺形态变化的动态对比研究

目的动态研究高碘与高酪氨酸对小鼠甲状腺形态结构变化的影响。方法将150只昆明种小鼠随机分为对照组(NI)、高碘组(HI)、高酪氨酸组(Htyr)、高碘高酪氨酸组(HI+Htyr)和高碘模型组(HIM)5组。在实验10周、20周和30周时,测定小鼠甲状腺绝对质量与相对质量,观察小鼠甲状腺组织形态变化。结果 20周时,HI组小鼠甲状腺相对质量显著高于NI组;30周时,HI+Htyr组小鼠甲状腺相对质量显著高于NI组。光镜结果显示,HI组呈现典型的胶质性甲状腺肿;同时HI+Htyr组也呈现出胶质性甲状腺肿的改变,但滤泡腔胶质减少。结论补充适量的酪氨酸可以减轻高碘对甲状腺组织的损伤作用,延缓昆明种小鼠甲肿的发生,但不能阻止高碘甲状腺肿的形成,说明在水碘为300μg/L的情况下,碘对甲状腺肿的作用是主要的,酪氨酸的作用是次要的。     

小鼠甲状腺肿发生率与碘的剂量反应关系

目的：研究小鼠甲状腺肿发生率与碘的剂量反应关系，确定引起小鼠10％、50％、90％甲状腺肿大率的水碘浓度，为动物高碘实验选用合适碘剂量提供参考依据。方法：用随机区组实验设计方法将初断乳昆明小鼠随机分为7组，用碘酸钾配制成含碘50μg/L的适碘对照组和250，500，1000，1500，2000，3000μg／L的高碘组，喂养100d后，观察各组甲状腺绝对、相对重量，组织形态学改变和甲状腺肿发生率.结果：①当水碘浓度在50－3000μg/L之间时，甲状腺绝对，相对重量与碘剂量呈明显的正相关，250μg/L组与对照比较差异有显著意义；②水碘浓度在250－3000μg／L之间时，小鼠甲状腺肿大率与碘剂量亦存在明显 的正相关关系，且引起小鼠10％、50％、90％甲状腺肿大率的水碘浓度分别为250，1500，3000μg/L。结论：饮水碘浓度在250－3000μg/L时，甲状腺肿大率与碘剂量呈明显的剂理反应关系，且引起小鼠10％、50％、90％甲状腺肿大率的水碘浓度分别为250，1500，3000μg/L，当饮水碘浓度为250μg/L时，即可引起小鼠胶质性甲状腺肿。     

Alterations to potassium fluxes in the heart during chronic dietary potassium depletion

Dietary K+ depletion in rabbits causes a loss of cellular K+ from skeletal muscle but not from cardiac muscle, and it has been suggested that this is due to a specific protective mechanism in the heart. Net uptake and efflux of 42K was investigated in the interventricular septum of the rabbit. Acute reductions in extracellular [K+] caused a loss of K+ from tissue of both normal and K+ depleted animals. In the K+ depleted group the relationship between [K+]e and net uptake was altered, so that the maximum rate of uptake was increased, and this was obtained at a lower [K+]e. There were no significant changes in K+ efflux. These results would be consistent with an adaptive change to the cardiac cell Na+ pump during chronic K+ depletion.     

碘酸钾和碘化钾对缺碘性甲状腺肿大鼠补碘效果的定量形态学观察

目的研究不同剂量的碘酸钾(KIO3)和碘化钾(KI)对缺碘性甲状腺肿(甲肿)大鼠的补碘效果。方法复制缺碘性甲肿大鼠动物模型,以适量碘(1倍,0.26mg/L)、5倍和50倍于适量碘的KIO3和KI6种方式补碘,1个月和3个月后测量大鼠甲状腺滤泡截面积,计算上皮细胞面积和胶质面积分别与视场面积比值。结果①6个补碘组的平均滤泡截面积均明显大于低碘组(LI组),但小于对照组(NI组),6个补碘组之间滤泡面积及其频数分布无明显差别;②6个补碘组滤泡上皮细胞面积与视场面积比,在补碘1个月时差异无统计学意义,但50倍KIO3和KI组上述比值有降低的趋势,3个月时该比值明显低于另外4个补碘组;③胶质面积与视场面积比,除LI组外各组间差异均无统计学意义;④相同补碘水平上,KIO3与KI组对上述各项测定结果的影响作用是一致的。结论不同剂量的KIO3和KI均对纠正缺碘性甲肿有效;相同补碘水平上,KIO3和KI对改善甲肿的效果是一致的;补大剂量的碘会造成甲状腺损伤;适宜剂量的KIO3对于纠正碘缺乏是安全有效的。     

Role of potassium in acid secretion

Potassium (K~+) ions are critical for the activation and catalytic cycle of the gastric H~+,K~+-ATPase, resulting in the secretion of hydrochloric acid into the parietal cell canaliculus. As both symptom, severity and esophageal mucosal damage in gastro-esophageal reflux disease (GERD) are related to the degree of acid exposure, K~+ is a logical target for approaches to inhibit acid production. The probable K~+ binding site on the gastric H~+,K~+-ATPase has recently been described and studies are elucidating how K~+ activates the enzyme. K~+ channels in the apical membrane of the parietal cell are implicated in the recycling of K~+ and, to date, three potential K~+ channels (KCNQ1, Kir2.1 and Kir4.1) have been identified. The channels represent theoretical sites for agents to control acid secretion but it will be difficult to develop selective blockers. An alternative strategy is to prevent K~+ from activating gastric H~+,K~+-ATPase; the potassiumcompetitive acid blocker (P-CAB) class inhibits acid secretion by binding at or near the K~+ binding site. Ongoing research is further defining the role of K~+ in the functioning of the gastric H~+,K~+-ATPase, as well as determining the clinical utility of agents directed toward this important cation.     

Effect of high potassium diet on endothelial function

Background and aimsIncreased potassium intake is related to reduced blood pressure (BP) and reduced stroke rate. The effect of increased dietary potassium on endothelial function remains unknown. The aim was to determine the effect of increased dietary potassium from fruit and vegetables on endothelial function.Methods and resultsThirty five healthy men and women (age 32 ± 12 y) successfully completed a randomised cross-over study of 2 × 6 day diets either high or low in potassium. Flow mediated dilatation (FMD), BP, pulse wave velocity (PWV), augmentation index (AI) and a fasting blood sample for analysis of Intercellular Adhesion Molecule-1 (ICAM-1), E-selectin, asymmetric dimethylarginine (ADMA) and endothelin-1 were taken on completion of each intervention. Dietary change was achieved by including bananas and potatoes in the high potassium and apples and rice/pasta in the low potassium diet. Dietary adherence was assessed using 6 day weighed food diaries and a 24 h urine sample. The difference in potassium excretion between the two diets was 48 ± 32 mmol/d (P = 0.000). Fasting FMD was significantly improved by 0.6% ± 1.5% following the high compared to the low potassium diet (P = 0.03). There were no significant differences in BP, PWV, AI, ICAM-1, ADMA or endothelin-1 between the interventions. There was a significant reduction in E-selectin following the high (Median = 5.96 ng/ml) vs the low potassium diet (Median = 6.24 ng/ml), z = −2.49, P = 0.013.ConclusionIncreased dietary potassium from fruit and vegetables improves FMD within 1 week in healthy men and women but the mechanisms for this effect remain unclear.Clinical trial registryACTRN12612000822886.     

心房颤动患者乙酰胆碱依赖性钾通道和快速延迟整流钾通道基因表达的研究

目的研究心房颤动(AF)患者心房组织中乙酰胆碱依赖性钾通道(Kach)和快速延迟整流钾通道(Kr)的基因表达。探讨AF时心房组织Kach和Kr的mRNA表达改变及其意义。方法自20例因风湿性心脏病或先天性心脏病接受外科手术的患者,于术中采取的右心耳标本分为2组,窦性心律(SR)组14例,慢性AF组6例,应用半定量逆转录聚合酶链反应(RTPCR)技术,检测心房组织Kach和Kr基因表达。结果心房组织中Kir34(Kach的一种成分)和KrmRNA的表达,与SR组051±005相比AF组029±005下调43%,差异有显著性(P<0001),而KrmRNA水平在SR组056±003和AF组057±003之间无明显改变,差异无显著性(P>005)。结论房颤患者KachmRNA表达下调,可能是心房肌细胞IKach密度减弱的分子基础。Kr转录水平无明显改变。     

血压盐敏感者内皮功能损伤及补钾的保护作用研究

目的通过观察血、尿-氧化氮（NO）水平的变化,探讨盐敏感者血管内皮功能损伤及补钾的保护作用。方法选39例年龄16～60岁、血压正常或血压轻度偏高者参与为期3周的慢性盐负荷及补钾试验,包括基线3天,低盐饮食、高盐饮食和高盐加补钾饮食各7天的研究。各个阶段测量体重、血压,并收集血、尿标本。结果盐敏感者血浆NO浓度和尿中NO水平在基线、低盐和高盐阶段均低于盐不敏感者;限盐后血、尿NO浓度增加,而高盐饮食后NO浓度显著减少;盐敏感者在高盐摄入的基础上大剂量口服补钾后血浆NO浓度、尿NO水平显著升高。结论盐敏感者尽管尚处在血压正常或血压轻度偏高阶段已存在一定程度的内皮功能损伤,且这种损伤与盐负荷相关联;大剂量补钾可能通过增加NO水平而改善盐敏感者的血管内皮功能。     

The carbohydrate metabolism of normal subjects during potassium depletion

Summary A potassium loss of 3–11% (6.0±2.7%) of total body potassium, was produced in 6 normal subjects during the course of a metabolic balance study of 13–16 days duration using a supplemented formula diet. This resulted in the development of a marked hypokaliaemic alkalosis. There were no significant changes of blood sugar, free fatty acid and plasma insulin concentrations during intravenous (0.5 g/kg) or oral (100 g) glucose tolerance tests for control and experimental periods.Chief of the laboratories of the municipal hospitals of Darmstadt.     

Associations between serum potassium and sodium levels and risk of hypertension: a community-based cohort study

Objective Several studies have examined the relationships between dietary potassium and sodium and hypertension, but few have evaluated the association between serum potassium or sodium and risk of incident hypertension. We therefore investigated the associations between serum potassium and sodium and risk of incident hypertension in a Chinese community-based population. Methods A total of 839 normotensive individuals without cardiovascular disease from the Chinese Multi-Provincial Cohort Study who took part in the baseline examination in 2007–2008 and the follow-up survey in 2012–2013 were included in this study. Odds ratios (OR) and 95% confidence intervals (95%CI) for baseline serum potassium and sodium in relation to the risk of new-onset hypertension were evaluated using multivariate logistic regression models. Results During five years of follow-up, 218 (26.0%) individuals progressed to hypertension. Logistic regression adjusting for multiple confounders showed that every 1 mEq/L increment in baseline serum potassium level was associated with a 75% increased risk of hypertension (OR: 1.75; 95%CI: 1.01–3.04; P = 0.04). Compared with adults with serum potassium level of 4.20–4.79 mEq/L, adults with level ≥ 4.80 mEq/L had an 84% increased risk of hypertension (OR: 1.84; 95%CI: 1.14–2.96; P = 0.01). There was no significant association between serum sodium and risk of hypertension (OR: 0.96; 95%CI: 0.89–1.04; P = 0.33). Conclusions Baseline serum potassium level, but not baseline serum sodium level, was positively related to the risk of incident hypertension in the Chinese population.